Neuron-Specific Enolase, but Not S100B or Myelin Basic Protein, Increases in Peripheral Blood Corresponding to Lesion Volume after Cortical Impact in Piglets

Costine, Beth A.; Quebeda-Clerkin, Patricia B.; Dodge, Carter P.; Harris, Brent T.; Hillier, Simon C.; Duhaime, Ann‐Christine

doi:10.1089/neu.2012.2428

Cited by 23 publications

(16 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cortical impact to the rostral gyrus was achieved via a spring-loaded device secured to the skull, and an indentor tip scaled to 1% of the volume of the brain was displaced over 4 msec. In injured animals, this produces a lesion size of 350 ± 50 mm 3 or approximately 10% of the volume of the contralateral hemisphere 1 week after injury that typically extends down into the gyral white matter [ 19 , 20 ]. This age of piglet corresponds developmentally to human toddlers [ 15 ].…”

Section: Methodsmentioning

confidence: 99%

Early inflammatory mediator gene expression in two models of traumatic brain injury: ex vivo cortical slice in mice and in vivo cortical impact in piglets

Graber

Costine

Hickey

2015

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundThe immunological response during the first 24 hours after traumatic brain injury (TBI) may be a critical therapeutic interval for limiting the secondary neuronal damage that is influenced by enhanced inflammatory mediator expression.MethodsTo gain further insight of the early injury response, we examined the expression of several inflammatory genes by real-time qPCR as a function of time or distance from injury in two distinct mammalian models: an ex vivo mouse cortical slice injury system and an in vivo piglet model of brain injury.ResultsInterleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), chemokine ligands 2 (CCL2), 3 (CCL3), 4 (CCL4), and prostaglandin-endoperoxide synthase 2 (PTGS2) mRNAs increased within 5 h after injury in mouse cortical slices. Chemokine and PTGS2 mRNAs remained elevated in slices at 24 h, whereas IL-1β and TNF-α expressions decreased from earlier peak levels. At 24 h after cortical injury in 1-month-old piglets, the expression of CCL2 mRNA was significantly increased in the lesion core and in the penumbra region. The expression of PTGS2, IL-1β, and TNF-α was variable among the piglets.ConclusionsThese in vitro and large animal models of cortical injury expand our understanding of the early timing and spread of the immunological response and can serve as preclinical systems to facilitate the discovery of therapeutic agents for TBI aimed at regulating inflammatory mediator expression.

show abstract

Section: Methodsmentioning

confidence: 99%

Early inflammatory mediator gene expression in two models of traumatic brain injury: ex vivo cortical slice in mice and in vivo cortical impact in piglets

Graber

Costine

Hickey

2015

J Neuroinflammation

View full text Add to dashboard Cite

show abstract

“…As with rodent models of CCI, when pigs are used the histopathological changes mirror what is seen in TBI patients, including but not limited to, deranged blood flow and changes to vasculature, ongoing neurodegeneration via a number of mechanisms, and edema. To date, pig models have been used to add to the evidence surrounding TBI biomechanics [52] and as part of an effort to identify clinically relevant biomarkers of underlying brain injury [53]. However, despite these efforts there is a relative dearth of normative data specific to pigs when compared to rodents [54].…”

Section: Pig-mentioning

confidence: 99%

The Controlled Cortical Impact Model of Experimental Brain Trauma: Overview, Research Applications, and Protocol

Osier¹,

Kline²,

Dixon³

2019

Springer Series in Translational Stroke Research

View full text Add to dashboard Cite

Controlled cortical impact (CCI) is a commonly used and highly regarded model of brain trauma that uses a pneumatically or electromagnetically controlled piston to induce reproducible and wellcontrolled injury. The CCI model was originally used in ferrets and it has since been scaled for use in many other species. This chapter will describe the historical development of the CCI model, compare and contrast the pneumatic and electromagnetic models, and summarize key short-and long-term consequences of TBI that have been gleaned using this model. In accordance with the recent efforts to promote high-quality evidence through the reporting of common data elements (CDEs), relevant study details-that should be reported in CCI studies-will be noted.

show abstract

“…By 1991, the device was adapted so that the model could be applied to rats ( 23 ). After translation to rats, CCI has since been applied to mice ( 24 – 26 ), swine ( 27 – 30 ), and non-human primates ( 31 ), as described in detail later in this review.…”

Section: Past and Present Applications: Model Overview Development mentioning

confidence: 99%

The Controlled Cortical Impact Model: Applications, Considerations for Researchers, and Future Directions

2016

View full text Add to dashboard Cite

Controlled cortical impact (CCI) is a mechanical model of traumatic brain injury (TBI) that was developed nearly 30 years ago with the goal of creating a testing platform to determine the biomechanical properties of brain tissue exposed to direct mechanical deformation. Initially used to model TBIs produced by automotive crashes, the CCI model rapidly transformed into a standardized technique to study TBI mechanisms and evaluate therapies. CCI is most commonly produced using a device that rapidly accelerates a rod to impact the surgically exposed cortical dural surface. The tip of the rod can be varied in size and geometry to accommodate scalability to difference species. Typically, the rod is actuated by a pneumatic piston or electromagnetic actuator. With some limits, CCI devices can control the velocity, depth, duration, and site of impact. The CCI model produces morphologic and cerebrovascular injury responses that resemble certain aspects of human TBI. Commonly observed are graded histologic and axonal derangements, disruption of the blood–brain barrier, subdural and intra-parenchymal hematoma, edema, inflammation, and alterations in cerebral blood flow. The CCI model also produces neurobehavioral and cognitive impairments similar to those observed clinically. In contrast to other TBI models, the CCI device induces a significantly pronounced cortical contusion, but is limited in the extent to which it models the diffuse effects of TBI; a related limitation is that not all clinical TBI cases are characterized by a contusion. Another perceived limitation is that a non-clinically relevant craniotomy is performed. Biomechanically, this is irrelevant at the tissue level. However, craniotomies are not atraumatic and the effects of surgery should be controlled by including surgical sham control groups. CCI devices have also been successfully used to impact closed skulls to study mild and repetitive TBI. Future directions for CCI research surround continued refinements to the model through technical improvements in the devices (e.g., minimizing mechanical sources of variation). Like all TBI models, publications should report key injury parameters as outlined in the NIH common data elements (CDEs) for pre-clinical TBI.

show abstract

Neuron-Specific Enolase, but Not S100B or Myelin Basic Protein, Increases in Peripheral Blood Corresponding to Lesion Volume after Cortical Impact in Piglets

Cited by 23 publications

References 36 publications

Early inflammatory mediator gene expression in two models of traumatic brain injury: ex vivo cortical slice in mice and in vivo cortical impact in piglets

Early inflammatory mediator gene expression in two models of traumatic brain injury: ex vivo cortical slice in mice and in vivo cortical impact in piglets

The Controlled Cortical Impact Model of Experimental Brain Trauma: Overview, Research Applications, and Protocol

The Controlled Cortical Impact Model: Applications, Considerations for Researchers, and Future Directions

Contact Info

Product

Resources

About